Uteroplacental insufficiency and reducing litter size alters skeletal muscle mitochondrial biogenesis in a sex-specific manner in the adult rat

Wadley, Glenn D.; Siebel, Andrew L.; Cooney, Gregory J.; McConell, Glenn K.; Wlodek, Mary E.; Owens, Julie A.

doi:10.1152/ajpendo.00037.2008

Cited by 54 publications

(143 citation statements)

References 42 publications

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“…This observation was already made in skeletal muscle where mitochondrial metabolic characteristics and biogenesis were altered to a greater extent in male compared with female rats following in utero placental insufficiency (21,22,63). Moreover, long-term consequences of a maternal LP diet on glucose tolerance developed earlier in male than in female offspring (8,13).…”

Section: Discussionmentioning

confidence: 75%

Maternal low-protein diet alters pancreatic islet mitochondrial function in a sex-specific manner in the adult rat

Theys

Bouckenooghe

Ahn

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Theys N, Bouckenooghe T, Ahn M-T, Remacle C, Reusens B. Maternal low-protein diet alters pancreatic islet mitochondrial function in a sex-specific manner in the adult rat. Am J Physiol Regul Integr Comp Physiol 297: R1516 -R1525, 2009. First published September 16, 2009; doi:10.1152/ajpregu.00280.2009.-Mitochondrial dysfunction may be a long-term consequence of a poor nutritional environment during early life. Our aim was to investigate whether a maternal low-protein (LP) diet may program mitochondrial dysfunction in islets of adult progeny before glucose intolerance ensues. To address this, pregnant Wistar rats were fed isocaloric diets containing either 20% protein (control) or 8% protein (LP diet) throughout gestation. From birth, offspring received the control diet. The mitochondrial function was analyzed in islets of 3-mo-old offspring. Related to their basal insulin release, cultured islets from both male and female LP offspring presented a lower response to glucose challenge and a blunted ATP production compared with control offspring. The expression of malate dehydrogenase as well as the subunit 6 of the ATP synthase encoded by mitochondrial genome (mtDNA) was lower in these islets, reducing the capacity of ATP production through the Krebs cycle and oxidative phosphorylation. However, mtDNA content was unchanged in LP islets compared with control. Several consequences of protein restriction during fetal life were more marked in male offspring. Only LP males showed an increased reactive oxygen species production associated with a higher expression of mitochondrial subunits of the electron transport chain NADH-ubiquinone oxireductase subunit 4L, an overexpression of peroxisome proliferator-activated receptor-␥ and uncoupling protein-2, and a strongly reduced beta-cell mass. In conclusion, mitochondrial function is clearly altered in islets from LP adult offspring in a sex-specific manner. That may provide a cellular explanation for the earlier development of glucose intolerance in male than in female offspring of dams fed an LP diet. developmental programming; malnutrition; metabolic syndrome; insulin secretion EPIDEMIOLOGICAL AND EXPERIMENTAL evidence shows a convincing relationship between a poor intrauterine nutritional environment and the subsequent development of metabolic disorders like insulin resistance, obesity, and cardiovascular disease in adulthood (11,12). The original concept of fetal programming of Type 2 diabetes mellitus (T2DM) was proposed by Hales et al. (12) who found in a cohort of adult men who had been smaller at birth that they were six times more prone to develop T2DM compared with individuals heavier at birth. These first epidemiological clues of programming have been largely replicated in many studies throughout the world (17, 27, 61). Currently, this concept is widely accepted, but the mechanistic basis is unclear.Recently, attention has focused on the involvement of mitochondria as putative targets linking physiological and molecular consequences of environmental disorders du...

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Section: Discussionmentioning

confidence: 75%

Maternal low-protein diet alters pancreatic islet mitochondrial function in a sex-specific manner in the adult rat

Theys

Bouckenooghe

Ahn

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Since we have previously observed marked sex differences in a range of metabolic and cardiovascular outcomes in adult rats following uteroplacental insufficiency (20,29,31), it is possible there could be similar sex-specific effects on the expression of genes in the mitochondrial biogenesis pathway, GLUTs and antioxidant enzymes during cardiac development in growth restricted rats.…”

mentioning

confidence: 98%

“…Using well-established rodent models of uteroplacental insufficiency, our group, and others, have shown that growth restriction in prenatal and/or postnatal life adversely impacts on later metabolic and cardiovascular health in adulthood, including hypertension (27,31,32), cardiac hypertrophy (32), myocardial insulin resistance (26), impaired glucose tolerance (20), reduced cardiomyocyte number (5), and reduced expression of genes regulating mitochondrial biogenesis (synthesis) in skeletal muscle (29).…”

mentioning

confidence: 99%

“…However, there are conflicting data as to whether PGC-1␣ mRNA is upregulated at all during cardiac development of the rat (11,23); while very little is known about the expression of other mitochondrial biogenesis genes (i.e., NRF-2, mtTFA, and COX) during this time. We have reported that uteroplacental insufficiency, which results in restriction of both prenatal and postnatal growth (Restricted) (29,32,33), reduces PGC-1␣ expression and other genes involved with mitochondrial biogenesis, including mtTFA and COX in the skeletal muscle of adult rats (29).…”

mentioning

confidence: 99%

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Growth restriction in the rat alters expression of metabolic genes during postnatal cardiac development in a sex-specific manner

Wadley

McConell

Goodman

et al. 2013

Physiological Genomics

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“…Both F1 male and female offspring have organ deficits, but only F1 male offspring develop hypertension and metabolic dysfunction in adult life (Wadley et al 2008, Moritz et al 2009). During late gestation, F1 female growth-restricted offspring become glucose intolerant, develop glomerular hypertrophy and have modifications in uterine artery function (Mazzuca et al 2010, Gallo et al 2012b.…”

Section: Introductionmentioning

confidence: 99%

Low female birth weight and advanced maternal age programme alterations in next-generation blastocyst development

et al. 2015

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Low birth weight is associated with an increased risk for adult disease development with recent studies highlighting transmission to subsequent generations. However, the mechanisms and timing of programming of disease transmission to the next generation remain unknown. The aim of this study was to examine the effects of low birth weight and advanced maternal age on second-generation preimplantation blastocysts. Uteroplacental insufficiency or sham surgery was performed in late-gestation WKY pregnant rats, giving rise to first-generation (F1) restricted (born small) and control offspring respectively. F1 control and restricted females, at 4 or 12 months of age, were naturally mated with normal males. Second-generation (F2) blastocysts from restricted females displayed reduced expression of genes related to growth compared with F2 control (P!0.05). Following 24 h culture, F2 restricted blastocysts had accelerated development, with increased total cell number, a result of increased trophectoderm cells compared with control (P!0.05). There were alterations in carbohydrate and serine utilisation in F2 restricted blastocysts and F2 restricted outgrowths from 4-month-old females respectively (P!0.05). F2 blastocysts from aged restricted females were developmentally delayed at retrieval, with reduced total cell number attributable to reduced trophectoderm number with changes in carbohydrate utilisation (P!0.05). Advanced maternal age resulted in alterations in a number of amino acids in media obtained from F2 blastocyst outgrowths (P!0.05). These findings demonstrate that growth restriction and advanced maternal age can alter F2 preimplantation embryo physiology and the subsequent offspring growth.

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Uteroplacental insufficiency and reducing litter size alters skeletal muscle mitochondrial biogenesis in a sex-specific manner in the adult rat

Abstract: Wadley GD, Siebel AL, Cooney GJ, McConell GK, Wlodek ME, Owens JA. Uteroplacental insufficiency and reducing litter size alters skeletal muscle mitochondrial biogenesis in a sex-specific manner in the adult rat.

Cited by 54 publications

References 42 publications

Maternal low-protein diet alters pancreatic islet mitochondrial function in a sex-specific manner in the adult rat

Maternal low-protein diet alters pancreatic islet mitochondrial function in a sex-specific manner in the adult rat

Growth restriction in the rat alters expression of metabolic genes during postnatal cardiac development in a sex-specific manner

Low female birth weight and advanced maternal age programme alterations in next-generation blastocyst development

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